Computational Fluid Dynamics Laboratory

Transition to Turbulence in Stenotic Blood Vessels


Atherosclerosis, a cardiovascular disease of the larger arteries, is the primary cause of heart disease and stroke. In the United States alone, statistics released by the American Heart Association estimated that more than 70 million Americans have one or more forms of cardiovascular disease, with coronary heart disease being the single leading cause of death, claiming almost 20% of all deaths in 2002 alone. Atherosclerosis is a progressive disease initiated by localized fatty streak lesions within the arteries occurring as early as childhood. Over decades, these lesions can develop into more complex plaques large enough to significantly block blood flow within the circulatory system. This local restriction of the artery is known as an arterial stenosis. Plaque deposition is most common in the aorta, coronary arteries, and carotid arteries; and, as one might expect, the presence of a stenosis can lead to serious health risks.

Stenoses are commonly characterized as a percentage reduction in diameter or area of the host vessel and are considered clinically significant when the reduction is greater than 75% by area. The progression of a low-level arterial blockage into a critical stenosis is in itself the result of complex non-linear interactions between factors such as flow conditions, wall compliance, and biological responses. The image below shows a cartoon of an arterial stenosis.


Direct Numerical Simulation of Stenotic Flows

Direct numerical simulations (DNS) of steady and pulsatile flow through 75% (by area reduction) stenosed tubes have been performed, with the motivation of understanding the biofluid dynamics of actual stenosed arteries. The spectral-element method, providing geometric flexibility and high-order spectral accuracy, was employed for the simulations. Under both steady and pulsatile inlet flow conditions, DNS predicted a laminar flowfield downstream of an axisymmetric stenosis and comparison to previous experiments showed good agreement in the immediate post-stenotic region. However, the introduction of a geometric perturbation at the stenosis throat, in the form of an eccentricity that was only 5% of the main vessel diameter, resulted in jet breakdown and transition to turbulence in the post-stenotic flowfield. In the case of steady inlet flow, transition was accomplished by the breaking up of streamwise, hairpin vortices into a localized turbulent spot.

Under pulsatile conditions, transition was achieved as a starting vortex structure, that formed during early acceleration, broke up into elongated streamwise structures that subsequently underwent turbulent breakdown during peak inlet flow, confirmed by turbulent statistics and broadband velocity spectra. Past the mid-deceleration phase, through to minimum flow, the inlet flow lost its momentum and the flowfield began to relaminarize. The start of acceleration in the following cycle saw a recurrence of the entire process of localized, periodic transition to turbulence. The animation below shows the evolution of vortex structures (colored by pressure) during a pulsatile flow cycle.


Wall shear stress (WSS) magnitudes at the stenosis throat exceeded upstream levels by more than a factor of thirty but significantly lower WSS levels accompanied the flow separation zones that formed immediately downstream. Transition to turbulence manifested itself in large temporal and spatial gradients of wall shear stress, with the turbulent region also witnessing a sharp amplification in WSS magnitudes.

Watch a beautiful animation showing cross-sections of velocity contours (gray scale) in eccentric stenosis case highlighting transition of eccentric stenotic jet from laminar to turbulent flow with enhanced mixing across the vessel.

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Watch a another beautiful animation showing cross-sections of velocity contours (gray scale) in eccentric stenosis case highlighting the recirculation zone region and increases near-vessel residence time important for further plaque development possibly leading to multiple and complex vulnerable plaque susceptible to rupture.
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